The p53 tumor suppressor inhibits transcription of the TATA-less mouse DP1 promoter

被引:24
作者
Gopalkrishnan, RV
Lam, EWF
Kedinger, C
机构
[1] Univ Louis Pasteur Strasbourg 1, CNRS, INSERM, Inst Genet & Biol Mol & Cellulaire, F-67404 Illkirch Graffenstaden, France
[2] St Marys Hosp, Imperial Coll, Sch Med, Dept Med Microbiol, London W2 1PG, England
[3] St Marys Hosp, Imperial Coll, Sch Med, Ludwig Inst Canc Res, London W2 1PG, England
关键词
D O I
10.1074/jbc.273.18.10972
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cell cycle progression is subject to several regulatory controls, of which the p53 protein plays a major role in growth arrest, subsequent to the detection of cellular aberrations. It is well documented that p53 has the ability to inhibit transcription driven by several promoters, possibly via distinct mechanisms. In this report, we show that expression of the cell cycle regulatory transcription factor DP1 is strongly inhibited by p53, at the level of transcription and probably through the basal TATA-less promoter. This inhibitory activity has a relative specificity for the DP1 promoter compared with the functionally related E2F1 promoter or unrelated promoters such as those of the transcription factor ATFa or the thymidine kinase gene. Inhibition of DPI transcription has implications in one of the several possible mechanisms through which p53 induces cell cycle arrest.
引用
收藏
页码:10972 / 10978
页数:7
相关论文
共 67 条
  • [1] TRANSCRIPTIONAL CONTROL BY E2F
    ADAMS, PD
    KAELIN, WG
    [J]. SEMINARS IN CANCER BIOLOGY, 1995, 6 (02) : 99 - 108
  • [2] DP-1 - A CELL-CYCLE-REGULATED AND PHOSPHORYLATED COMPONENT OF TRANSCRIPTION FACTOR DRTF1/E2F WHICH IS FUNCTIONALLY IMPORTANT FOR RECOGNITION BY PRB AND THE ADENOVIRUS E4-ORF-6/7 PROTEIN
    BANDARA, LR
    LAM, EWF
    SORENSEN, TS
    ZAMANIAN, M
    GIRLING, R
    LATHANGUE, NB
    [J]. EMBO JOURNAL, 1994, 13 (13) : 3104 - 3114
  • [3] REPORTER CONSTRUCTS WITH LOW BACKGROUND ACTIVITY UTILIZING THE CAT GENE
    BOSHART, M
    KLUPPEL, M
    SCHMIDT, A
    SCHUTZ, G
    LUCKOW, B
    [J]. GENE, 1992, 110 (01) : 129 - 130
  • [4] Further characterisation of the p53 responsive element - Identification of new candidate genes for trans-activation by p53
    Bourdon, JC
    DeguinChambon, V
    Lelong, JC
    Dessen, P
    May, P
    Debuire, B
    May, E
    [J]. ONCOGENE, 1997, 14 (01) : 85 - 94
  • [5] MODULATION OF ACTIVITY OF THE PROMOTER OF THE HUMAN MDR1 GENE BY RAS AND P53
    CHIN, KV
    UEDA, K
    PASTAN, I
    GOTTESMAN, MM
    [J]. SCIENCE, 1992, 255 (5043) : 459 - 462
  • [6] Dimri GP, 1996, MOL CELL BIOL, V16, P2987
  • [7] MICE DEFICIENT FOR P53 ARE DEVELOPMENTALLY NORMAL BUT SUSCEPTIBLE TO SPONTANEOUS TUMORS
    DONEHOWER, LA
    HARVEY, M
    SLAGLE, BL
    MCARTHUR, MJ
    MONTGOMERY, CA
    BUTEL, JS
    BRADLEY, A
    [J]. NATURE, 1992, 356 (6366) : 215 - 221
  • [8] DubsPoterszman MC, 1995, ONCOGENE, V11, P2445
  • [9] DEFINITION OF A CONSENSUS BINDING-SITE FOR P53
    ELDEIRY, WS
    KERN, SE
    PIETENPOL, JA
    KINZLER, KW
    VOGELSTEIN, B
    [J]. NATURE GENETICS, 1992, 1 (01) : 45 - 49
  • [10] ELDEIRY WS, 1994, CANCER RES, V54, P1169